Friday, November 06, 2009
Image by brunosan.
One of the most interesting (and most complicated) things about obesity is its very strong neural component. Now of course at its most basic level, body weight comes down to the balance of energy intake versus energy expenditure. Unfortunately, many aspects of this energy balance equation are outside the influence of conscious control. The brain is constantly sensing nutrients like glucose, and hormones like leptin and insulin in order to determine current energy stores, and using this information to adjust energy intake and energy expenditure as needed. It does this by influencing our hunger and satiety, in order to keep body weight around a chosen set-point, or to return to a set-point after a short-term perturbation (e.g. a crash diet). So even though an individual may have decided to cut back on their caloric intake and increase their physical activity levels, this is obviously not so easy if their brain is making them feel hungry and lethargic all the time. As you might expect, research suggests that this neural control of energy intake and energy expenditure plays an extremely important role in obesity, weight maintenance, and weight reduction.
One study that nicely illustrates the link between obesity and these neural mechanisms was performed by Dr C.W. le Roux and colleagues at the Imperial College of London titled "Attenuated Peptite YY Release in Obese Subjects is Associated with Reduced Satiety". Peptide YY (aka PYY) is a hormone which is secreted from the intestines in response to a meal, and through its effects on the brain has a strong influence on satiety. The larger a meal, the more PYY that is released and the fuller you feel. In this study, Dr le Roux and colleagues examined the PYY response in lean and obese individuals. Each subject received 6 different meals throughout the course of the study, varying in both size and caloric density. They report that for a given caloric load, obese individuals had a dramatically lower PYY response, which was matched by a lower feeling of fullness. In fact, obese individuals required roughly double the meal calorie content to match the PYY levels in the lean subjects. However, when the authors injected PYY into the subjects, it produced similar feelings of fullness in both the lean and obese participants. These results suggest that PYY secretion is lowered in obese individuals, but unlike leptin, central sensitivity to PYY does not appear to be affected.
Unfortunately, the $64,000 question remains - does obesity cause changes in PYY secretion, or does a deficiency in PYY secretion cause obesity? That question, to my knowledge, has yet to be definitively answered (although I'm going to guess it's a bit of both, which always seems to be a safe bet with this type of thing). The point, however, is that body weight management is not quite so simple as telling someone to eat less and move more, although those behaviors are still the end goal. If an individual never feels full, they are obviously going to find it more difficult to lose weight than someone who always feels full. That's one of the reasons why gastric bypass is so effective - with a smaller stomach, people feel full much sooner! The more that we know about the neural control of long-term energy balance, the more effective strategies we will be able to develop to help prevent or reduce obesity in the future.
If you find the role of the brain in obesity as interesting as I do, you may be interested in a free presentation by Dr Barry Levin at the University of Ottawa Health Sciences Campus at 1pm on Nov 20. Dr Levin is an internationally renowned researcher on the area of the brain-obesity connection, and it looks to be a terrific presentation. It is open to the public, so if you live within driving distance of Ottawa and are interested in obesity research, this event might be for you. For more info on Dr Levin's presentation, please click here.
Have a great weekend,
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le Roux, C. (2005). Attenuated Peptide YY Release in Obese Subjects Is Associated with Reduced Satiety Endocrinology, 147 (1), 3-8 DOI: 10.1210/en.2005-0972
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